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Tumors originating from thyroid follicular cells are the most common endocrine tumors, with rising incidence. Despite a generally good prognosis, up to 20% of patients experience recurrence and persistence, highlighting the need to identify the underlying molecular mechanisms. <i>Dicer1</i> has been found to be altered in papillary thyroid cancer (PTC). Studies suggest that <i>Dicer1</i> functions as a haploinsufficient tumor suppressor gene: partial loss promotes tumorigenesis, while complete loss prevents it. To investigate the effects of partial or total <i>Dicer1</i> loss in PTC in vitro, we generated stable <i>Dicer1</i> (+/−) cell lines from TPC1 using CRISPR-Cas9, though no <i>Dicer1</i> (−/−) lines could be produced. Therefore, siRNA against <i>Dicer1</i> was transfected into <i>Dicer1</i> (+/−) cell lines to further decrease its expression. Transcriptomic analysis revealed changes in proliferation and cell locomotion. BrdU staining indicated a slow-down of the cell cycle, with fewer cells in S phase and more in G0-G1-phase. Additionally, transwell assays showed decreased invasion and migration after <i>Dicer1</i> knockdown by siRNA. Moreover, <i>Dicer1</i> overexpression led to decreased proliferation, invasion, and increased apoptosis. Our findings deepen the understanding of <i>Dicer1</i>’s role in thyroid cancer, demonstrating that both complete elimination and overexpression of <i>Dicer1</i> inhibit thyroid oncogenesis, highlighting <i>Dicer1</i> as a promising target for novel therapeutic strategies.